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Updated: Mar 7, 2026

Biventricular Assessment of Cardiac Function and Pressure-Volume Loops by Closed-Chest Catheterization in Mice
Published on: June 15, 2020
Relationships Between Left Ventricular Structure and Function According to Cardiac MRI and Cardiac Biomarkers in
Bryan A Ross1, Ron Wald2, Marc B Goldstein2
1Terrence Donnelly Heart Centre, St Michael's Hospital, Toronto, Ontario, Canada; University of Toronto, Toronto, Ontario, Canada.
Background:
We sought to assess the relationships between left ventricular (LV) remodelling and the mechanical and uremic stressors in hemodialysis patients.
Methods:
In this prospective 2-centre cohort study, 67 prevalent hemodialysis patients were followed for 1 year. Data on routine bloodwork and predialysis blood pressure (BP) measurements were collected over a 12-week period. LV end-diastolic volume (LVEDV) and LV mass (LVM) were measured using cardiac magnetic resonance imaging and indexed. High-sensitivity troponin-I (hsTnI), N-terminal pro-brain natriuretic peptide (NT-proBNP), fibroblast growth factor 23 (FGF-23), and high-sensitivity C-reactive protein (hsCRP) were also measured. All study procedures were performed at baseline and at 1 year. We examined the relationships between LV remodelling and (1) NT-proBNP and hsTnI (LV stretch and injury); (2) ultrafiltration volume (UFV) and interdialytic weight gain (IDWT; volume overload); (3) predialysis BP measurements (pressure overload); and (4) biomarkers of inflammation (hsCRP) and fibrosis (FGF-23).
Results:
LVEDV was significantly associated with UFV and with IDWT, at baseline as well as at 1 year. NT-proBNP was significantly and negatively correlated with UFV and IDWT, respectively, at 1 year. There were significant correlations between systolic BP and LVM index, at baseline and at 1 year as well as longitudinally. Systolic BP was the only parameter longitudinally correlated with LVM/LVEDV. hsTnI was not associated with urea, parathyroid hormone, calcium, phosphorus, FGF-23, hsCRP, or hemoglobin.
Conclusions:
We did not observe significant relationships between myocardial injury and markers of fibrosis, inflammation, and LV remodelling. Elevated predialysis systolic BP, which might represent a common mediator of pressure and volume overload, appears to be a dominant stimulus for LV remodelling.
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